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Three strikes to knock cancer out BRCA1 andBRCA2 are tumor-suppressor genes, and patients with mutations in these genes are predisposed to breast, ovarian, and other cancers. BecauseBRCA1 andBRCA2 mutations affect pathways involved in DNA break repair, these patients' tumors are usually vulnerable to treatments that further damage DNA repair, such as poly(ADP-ribose) polymerase (PARP) inhibitors, but they can acquire resistance to therapy. Using a genome-wide screening approach, Fuggeret al. identified a protein called DNPH1 as a “nucleotide sanitizer” that prevents the incorporation of abnormal nucleotides into DNA (see the Perspective by Kriaucionis). The authors examined its mechanism of action and demonstrated how it can be targeted to expedite the killing ofBRCA1 -mutant cancer cells in combination with PARP inhibitor treatment.Science , this issue p.156 ; see also p.127

Targeting the nucleotide salvage factor DNPH1 sensitizes BRCA -deficient cells to PARP inhibitors